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This was confirmed by time studies where 1) a 2 min HIV-pretreatment followed by washing before stimulation was sufficient to inhibit PHA induced proliferation of normal lymphocytes, and 2) addition of HIV to PHA prestimulated lymphocytes failed to inhibit proliferation, e.g., there was no effect on preactivated lymphocytes[6].

High responders to life stress had significantly less response to PHA, and high responders to cold pressor stress had lower PWM responses [8].

An analysis of all aphidicolin-inducible breakpoints has been carried out in PHA stimulated T-lymphocytes of five patients with classical Rett syndrome, their mothers and a group of age matched controls [9].

The only difference in the immunological status of the patients who had experienced a stressful life event in the previous twelve months and those that had not, involved PHA mitogenic activity which was significantly lower after a stressful event[10].

The percent change achieved by the addition of indomethacin to a PHA-induced proliferative response was significantly increased in patients with cirrhosis compared with controls (p less than 0.001) [14].

Blastogen A induced peak uptake of thymidine during day 6 of tissue culture whereas PHA induced peak uptake during day 5 and tetanus during day 8 [15].

We found no putative disease mutations in any of these proteins in subjects with non-LMNA FPLD, but, through the screening of diseased and normal subjects, we identified several single-nucleotide polymorphisms (SNPs); specifically, five SNPs in LMNB1 and four SNPs in LBR[20].

1. LBR has a nucleoplasmic, amino-terminal domain of approximately 200 amino acids followed by a carboxyl-terminal domain similar in sequence to yeast and plant sterol reductases [18].

To test the effects of C14 reductase inhibitors on LBR activity, we constructed EMY54, an ergosterol-requiring strain that is devoid of both sterol C8-C7 isomerase and sterol C14 reductase activities [25].

Cross-linking experiments, however, illustrate a tight association of HA95 with LBR and LAP2 only [30].

The modular domain organization of HP1-type proteins and LBR can explain some of the diverse protein-protein interactions at the chromatin-lamina-membrane interface of the nuclear envelope[31].

We also define a new class of variant PxVxL CSD-binding motifs in Sp100A, LBR, and ATRX[32].

Interestingly, emerin and LBR initially accumulated at distinct, separate locations, but then became uniform 8 minutes after the onset of anaphase, concurrent with the recovery of nuclear import function [33].